Joanna Bonior

Obesity is a global problem, increasing interest in adipose tissue (AT) biology. One of the techniques for analyzing visceral adipose tissue (VAT) and phase angle (PhA) is bioelectrical impedance analysis (BIA). PhA is considered an indicator of cell integrity and health and can be a prognostic marker in diseases and clinical conditions. The aim of the study was to assess the nutritional status and level of visceral fat area (VFA) to investigate the association between phase angle (PhA) and content of visceral adipose tissue in young adults. Our cohort consisted of 292 young adults (18–25), both sexes. Body composition was performed by the inBody 770 analyzer. We confirmed the relationship between PhA and gender (female vs. male: 5.3 vs. 6.5; p < 0.001) and BMI (female vs. male: 22.56 kg/m² vs. 23.78 kg/m²; p = 0.013). A total of 20.2% of examined students had a VFA of more than 100 cm² (Visceral Obesity, VO). We demonstrated a dependence between VFA and PhA value (PhA = 5.4 (VFA > 100 cm²) vs. PhA = 5.7 (VFA < 100 cm²), p = 0.003). Students with VO and normal BMI had a significantly lower PhA than those with VO and BMI ≥ 30 kg/m² (p = 0.021). PhA may be a useful indicator for assessing nutritional status and physiological differences related to gender, BMI, and visceral obesity in young adults.

Osteosarcopenia, characterized by concurrent bone loss and muscle wasting, significantly impacts mobility and quality of life. While age-related primary osteosarcopenia is well-studied, secondary osteosarcopenia (SOS) caused by chronic diseases remains poorly understood, particularly in young individuals. The present study aimed to comprehensively characterize musculoskeletal alterations associated with SOS using a juvenile porcine model of cerulein-induced chronic pancreatitis. Femoral bone analysis included densitometry, mechanical testing, histomorphometry, and serum bone turnover markers. The quadriceps femoris muscle was evaluated through histological analysis and gene expression profiling of antioxidant enzymes and apoptotic regulators. Animals with SOS showed significantly reduced femoral BMD compared to controls, with altered cortical geometry and compromised mechanical properties. Trabecular bone analysis revealed classic osteoporotic changes with decreased bone volume fraction. Negative changes were also observed in the growth plate morphology, indicating impaired endochondral ossification. Bone turnover markers indicated elevated bone resorption and altered formation. Muscle analysis demonstrated sarcopenic changes with selective atrophy of fast-twitch type II fibers and increased fiber density. At the molecular level, SOS muscles exhibited downregulated expression of CAT and CASP3, suggesting muscle atrophy predominantly mediated by oxidative stress and caspase-independent proteolysis rather than classical apoptosis. In conclusion, chronic pancreatitis in young pigs induces coupled bone and muscle degeneration consistent with secondary osteosarcopenia, demonstrating that muscle–bone crosstalk dysfunction occurs early in chronic inflammatory disease.